Bogomoletz Institute of Physiology

Kiev, Ukraine

Bogomoletz Institute of Physiology

Kiev, Ukraine
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Kopach O.,Bogomoletz Institute of Physiology | Voitenko N.,Bogomoletz Institute of Physiology | Voitenko N.,Moscow Institute of Physics and Technology
Brain Research Bulletin | Year: 2013

Extrasynaptic AMPA receptors (AMPARs) are widely expressed in the brain, spinal cord and periphery. These receptors are critically involved in activity-dependent synaptic transmission and changes in their functioning are causally linked to multiple neuropathologies in the central nervous system (CNS). However, most studies in this field have been concentrated on elucidating synaptic AMPAR functioning, leaving a possible involvement of an extrasynaptic pool of AMPARs in normal and pathological signaling open for consideration.Here, we review the present evidence for extrasynaptic AMPAR function in the dorsal horn neurons of the spinal cord, linking these receptors to neurotransmission and non-synaptic signaling in this part of the CNS. In addition, we summarize current knowledge about the role of extrasynaptic AMPARs in the development and maintenance of pain states during inflammation. This knowledge potentially suggests the development of alternative therapies to prevent and/or treat inflammatory pain. © 2012 Elsevier Inc.

Lushnikova I.,Bogomoletz Institute of Physiology | Skibo G.,Bogomoletz Institute of Physiology | Muller D.,University of Geneva | Nikonenko I.,University of Geneva
Neuropharmacology | Year: 2011

Synaptic activity, such as long-term potentiation (LTP), has been shown to induce morphological plasticity of excitatory synapses on dendritic spines through the spine head and postsynaptic density (PSD) enlargement and reorganization. Much less, however, is known about activity-induced morphological modifications of inhibitory synapses. Using an in vitro model of rat organotypic hippocampal slice cultures and electron microscopy, we studied activity-related morphological changes of somatic inhibitory inputs triggered by a brief oxygen-glucose deprivation (OGD) episode, a condition associated with a synaptic enhancement referred to as anoxic LTP and a structural remodeling of excitatory synapses. Three-dimensional reconstruction of inhibitory axo-somatic synapses at different times before and after brief OGD revealed important morphological changes. The PSD area significantly and markedly increased at synapses with large and complex PSDs, but not at synapses with simple, macular PSDs. Activity-related changes of PSD size and presynaptic bouton volume developed in a strongly correlated manner. Analyses of single and serial sections further showed that the density of inhibitory synaptic contacts on the cell soma did not change within 1 h after OGD. In contrast, the proportion of the cell surface covered with inhibitory PSDs, as well as the complexity of these PSDs significantly increased, with less macular PSDs and more complex, segmented shapes. Together, these data reveal a rapid activity-related restructuring of somatic inhibitory synapses characterized by an enlargement and increased complexity of inhibitory PSDs, providing a new mechanism for a quick adjustment of the excitatory-inhibitory balance. This article is part of a Special Issue entitled 'Synaptic Plasticity & Interneurons'. © 2010 Elsevier Ltd. All rights reserved.

Cellular mechanisms of antinociceptive action of neuropeptide Y were investigated in substantia gelatinosa (SG) neurons in rat spinal cord slices. Somatic and synaptic effects of NPY were compared in two subpopulations of cells with different firing patterns, tonic (TFNs), and delayed firing (DFNs) neurons. For the study, TFNs were selected on morphological basis: they had appearance of central and radial but not islet cells, and are likely excitatory interneurons in dorsal horn networks. In their turn, DFNs were classified as radial and vertical cells. 0.3 μM NPY via Y1 receptors activated hyperpolarizing postsynaptic current of GIRK type in majority of TFNs (~77%) but not DFNs (~8%). Miniature synaptic currents in all neurons were seen as a mixture of excitatory (mEPSCs) and inhibitory (mIPSCs), the frequency of the former being ~5 times greater. The mEPSCs were mediated by glutamate receptors of AMPA subtype, while the dominant part of mIPSCs-by glycine receptors. In all cell types, NPY moderately depressed the frequency of both mEPSCs and mIPSCs; the effects occurred via Y2 and Y1 receptors, respectively. The data suggest that behavioral NPY-evoked antinociception is achieved via postsynaptic hyperpolarization of majority of TFNs (assumingly, excitatory interneurons) via Y1 receptors and depression of the mEPSCs via Y2 receptors. © 2012 Wiley Periodicals, Inc.

Gerasimenko J.V.,University of Cardiff | Gryshchenko O.,Bogomoletz Institute of Physiology | Ferdek P.E.,University of Cardiff | Stapleton E.,University of Cardiff | And 7 more authors.
Proceedings of the National Academy of Sciences of the United States of America | Year: 2013

Alcohol-related acute pancreatitis can be mediated by a combination of alcohol and fatty acids (fatty acid ethyl esters) and is initiated by a sustained elevation of the Ca2+ concentration inside pancreatic acinar cells ([Ca2+]i), due to excessive release of Ca2+ stored inside the cells followed by Ca2+ entry from the interstitial fluid. The sustained [Ca2+]i elevation activates intracellular digestive proenzymes resulting in necrosis and inflammation. We tested the hypothesis that pharmacological blockade of store-operated or Ca2+ release-activated Ca2+ channels (CRAC) would prevent sustained elevation of [Ca2+]i and therefore protease activation and necrosis. In isolated mouse pancreatic acinar cells, CRAC channels were activated by blocking Ca2+ ATPase pumps in the endoplasmic reticulum with thapsigargin in the absence of external Ca2+. Ca2+ entry then occurred upon admission of Ca2+ to the extracellular solution. The CRAC channel blocker developed by GlaxoSmithKline, GSK-7975A, inhibited store-operated Ca2+ entry in a concentrationdependent manner within the range of 1 to 50 μM (IC50 = 3.4 μM), but had little or no effect on the physiological Ca2+ spiking evoked by acetylcholine or cholecystokinin. Palmitoleic acid ethyl ester (100 μM), an important mediator of alcohol-related pancreatitis, evoked a sustained elevation of [Ca 2+]i, which was markedly reduced by CRAC blockade. Importantly, the palmitoleic acid ethyl ester-induced trypsin and protease activity as well as necrosis were almost abolished by blocking CRAC channels. There is currently no specific treatment of pancreatitis, but our data show that pharmacological CRAC blockade is highly effective against toxic [Ca2+]i elevation, necrosis, and trypsin/protease activity and therefore has potential to effectively treat pancreatitis.

Melnick I.V.,Bogomoletz Institute of Physiology
Synapse | Year: 2011

Substantia gelatinosa neurons display three main types of intrinsic firing behavior: tonic, adapting, and delayed onset. Here, voltage-gated currents expressed by delayed firing neurons were studied in nucleated patches obtained in spinal cord slices of 3-5 weeks-old rats. Inward Na+ current was negligible under these conditions and was usually occluded by superposition of much larger outward currents. Two kinds of outward currents were found, an A-type (KA) and delayed rectifier (KDR) potassium currents. KA activated rapidly (<1.5 ms at >-20 mV) and operated at subthreshold membrane potentials; voltages of steady-state half-maximal activation and inactivation were -38.7 and -87.2 mV, respectively. Inactivation was biexponential with a dominant fast component (∼90%, time constant ∼8 ms). KDR activated more slowly (<8 ms at >-20 mV), half-maximal activation was -23.6 mV, and decayed mono-exponentially with a time constant 70-110 ms. Maximal amplitudes of KA were almost 10-times larger than those of KDR, their respective densities were 8.5 and 0.97 μS μm-2. Tetraethylammonium, 5 mM, blocked KDR but not KA, whereas both currents were depressed by 5 mM 4-aminopyridine. In current-clamp recordings, 4-action potential but not tetraethylammonium abolished firing delay suggesting the causative role of KA. Thus, the predominance of fast KA over other somatic currents is a distinctive feature of delayed firing neurons among all other types of substantia gelatinosa neurons and likely explains the appearance of their typical firing delay. © 2010 Wiley-Liss, Inc.

Melnick I.V.,Bogomoletz Institute of Physiology | Price C.J.,University of Alberta | Colmers W.F.,University of Alberta
European Journal of Neuroscience | Year: 2011

Specialized hypothalamic neurons responding to rising extracellular glucose via increases or decreases in their electrical activity [glucose-excited (GE) and glucose-inhibited (GI) cells, respectively] have been reported in the hypothalamic arcuate, ventromedial and lateral nuclei. The hypothalamic paraventricular nucleus (PVN) is an important neurosecretory and preautonomic output nucleus. We tested whether parvocellular PVN neurons also possess glucosensing properties, using patch-clamp recording and immunocytochemistry. Putative neurosecretory (p-NS) and preautonomic (p-PA) cells were identified electrophysiologically. Although parvocellular neurons were insensitive to transitions from 10 to 2.5mm glucose, approximately 68% of p-PA cells responded directly to glucopenia (mimicked by a step to 0.2mm glucose) with an increased membrane conductance. Of these, approximately 24% hyperpolarized (accompanied by an outward current) and thus were GE, approximately 26% depolarized (with an inward current, thus GI) and approximately 18% did not change membrane potential. The concentration dependence of the glucose response was similar for both GE and GI cells (EC 50 of 0.67-0.7mm), but was steep, with Hill slopes of 3-4. The K ATP channel blockers glibenclamide and tolbutamide did not prevent, while the K ATP channel opener diazoxide did not mimic, the effects of low glucose on GE neurons. Moreover, the K ATP sulfonylurea receptor SUR1 was not detected in glucosensitive neurons. We conclude that the PVN contains previously unknown GE and GI cells that could participate in regulation of autonomic functions. GE neurons in the PVN sense ambient glucose via a unique mechanism, probably independent of K ATP channels, in contrast to neurons in other hypothalamic nuclei. © 2011 The Authors. European Journal of Neuroscience © 2011 Federation of European Neuroscience Societies and Blackwell Publishing Ltd.

News Article | December 27, 2016

The Biophysical Society has announced the winners of its international travel grants to attend the Biophysical Society's 61st Annual Meeting in New Orleans, February 11-15, 2017. The purpose of these awards is to foster and initiate further interaction between American biophysicists and scientists working in countries experiencing financial difficulties. Recipients of this competitive award are chosen based on scientific merit and their proposed presentation at the meeting. They will be honored at a reception on Sunday, February 12 at the Ernest N. Morial Convention Center. The 2017 recipients of the International Travel Award, along with their institutional affiliation and abstract title, are listed below. Ana F. Guedes, Institute of Molecular Medicine, Portugal, ATOMIC FORCE MICROSCOPY AS A TOOL TO EVALUATE THE RISK OF CARDIOVASCULAR DISEASES IN PATIENTS. Karishma Bhasne Mohali, Indian Institute of Science Education and Research (IISER), A TALE OF TWO AMYLOIDOGENIC INTRINSICALLY DISORDERED PROTEINS: INTERPLAY OF TAU AND α-SYNUCLEIN. Chan Cao, East China University of Science and Technology, DIRECT IDENTIFICATION OF ADENINE, THYMINE, CYTOSINE AND GUANINE USING AEROLYSIN NANOPORE. Venkata Reddy Chirasani, Indian Institute of Technology Madras, LIPID TRANSFER MECHANISM OF CETP BETWEEN HDL AND LDL: A COARSEGRAINED SIMULATION STUDY. Assaf Elazar, Weizmann Institute of Science, Israel, DECIPHERING MEMBRANE PROTEIN ENERGETICS USING DEEP SEQUENCING; TOWARDS ROBUST DESIGN AND STRUCTURE PREDICTION OF MEMBRANE PROTEINS. Manuela Gabriel, University of Buenos Aires, Argentina, 3D ORBITAL TRACKING OF SINGLE GOLD NANOPARTICLES: A NEW APPROACH TO STUDY VESICLE TRAFFICKING IN CHROMAFFIN CELLS. Farah Haque National Centre for Biological Sciences, India, A NEW HUMANIZED MOUSE MODEL FOR STUDYING INHERITED CARDIOMYOPATHIC MUTATIONS IN THE MYH7 GENE. Stephanie Heusser, Stockholm University, Switzerland, STRUCTURAL AND FUNCTIONAL EVIDENCE FOR MULTI-SITE ALLOSTERY MEDIATED BY GENERAL ANESTHETICS IN A MODEL LIGAND-GATED ION CHANNEL. Amir Irani, Massey University, New Zealand, HOMOGALACTURONANS ILLUMINATE THE ROLE OF COUNTERION CONDENSATION IN POLYELECTROLYTE TRANSPORT. Olfat Malak, University of Nantes, France, HIV-TAT INDUCES A DECREASE IN IKR AND IKS VIA REDUCTION IN PHOSPHATIDYLINOSITOL-(4,5)-BISPHOSPHATE AVAILABILITY. CONFORMATIONAL TRANSITION AND ASSEMBLY OF E.COLI CYTOLYSIN A PORE FORMING TOXIN BY SINGLE MOLECULE FLUORESCENCE. Sabrina Sharmin, Shizuoka University, Japan, EFFECTS OF LIPID COMPOSITIONS ON THE ENTRY OF CELL PENETRATING PEPTIDE OLIGOARGININE INTO SINGLE VESICLES. Xin Shi, East China University of Science and Technology, DIRECT OBSERVATION OF SINGLE BIOPOLYMER FOLDING AND UNFOLDING PROCESS BY SOLIDSTATE NANOPORE. Omar Alijevic, University of Lausanne, Switzerland, ANALYSIS OF GATING OF ACID-SENSING ION CHANNELS (ASICS) UNDER RAPID AND SLOW PH CHANGES. Swapna Bera, Bose Institute, India, BIOPHYSICAL INSIGHTS INTO THE MEMBRANE INTERACTION OF THE CORE AMYLOID-FORMING Aβ40 FRAGMENT K16-K28 AND ITS ROLE IN THE PATHOGENESIS OF ALZHEIMER'S DISEASE. Anais Cassaignau, University College London, United Kingdom, STRUCTURAL INVESTIGATION OF AN IMMUNOGLOBULIN DOMAIN ON THE RIBOSOME USING NMR SPECTROSCOPY. Bappaditya Chandra, Tata Institute of Fundamental Research, India, SECONDARY STRUCTURE FLIPPING CONNECTED TO SALT-BRIDGE FORMATION CONVERTS TOXIC AMYLOID-β40 OLIGOMERS TO FIBRILS. Gayathri Narasimhan, Cinvestav, Mexico, ANTIHYPERTROPHIC EFFECTS OF DIAZOXIDE INVOLVES CHANGES IN MIR-132 EXPRESSION IN ADULT RAT CARDIOMYCYTES. Giulia Paci, European Molecular Biology Laboratory, Germany, FOLLOWING A GIANT'S FOOTSTEPS: SINGLE-PARTICLE AND SUPER-RESOLUTION APPROACHES TO DECIPHER THE NUCLEAR TRANSPORT OF HEPATITIS B VIRUS CAPSIDS. Bizhan Sharopov, Bogomoletz Institute of Physiology National Academy of Sciences of Ukraine, DISSECTING LOCAL AND SYSTEMIC EFFECTS OF TRPV1 ON BLADDER CONTRACTILITY IN DIABETES. Chao Sun, East China Normal University, FUNCTION OF BACTERIORUBERIN IN ARCHAERHODOPSIN 4, FROM EXPRESSION TO CHARACTERIZATION. Matthew Batchelor, University of Leeds, United Kingdom STRUCTURAL DYNAMICS IN THE MYOSIN 7A SINGLE α-HELIX DOMAIN. Daniel Havelka, Czech Academy of Sciences, MICROVOLUME DIELECTRIC SPECTROSCOPY AND MOLECULAR DYNAMICS OF AMINO ACIDS. Ivan Kadurin, University College London, United Kingdom, INVESTIGATION OF THE PROTEOLYTIC CLEAVAGE OF α2δ SUBUNITS: A MECHANISTIC SWITCH FROM NHIBITION TO ACTIVATION OF VOLTAGE-GATED CALCIUM CHANNELS? Linlin Ma, University of Queensland, Australia, NOVEL HUMAN EAG CHANNEL ANTAGONISTS FROM SPIDER VENOMS. Ivana Malvacio, University of Cagliari, Italy, MOLECULAR INSIGHTS ON THE RECOGNITION OF SUBSTRATES BY THE PROMISCUOUS EFFLUX PUMP ACRB. Cristina Moreno Vadillo, Cardiovascular Research Institute Maastricht, Netherlands, RESTORING DEFECTIVE CAMP-DEPENDENT UPREGULATION IN LONG-QT SYNDROME TYPE-1 THROUGH INTERVENTIONS THAT PROMOTE IKS CHANNEL OPENING. Melanie Paillard, Claude Bernard University Lyon 1, France, TISSUE-SPECIFIC MITOCHONDRIAL DECODING OF CYTOPLASMIC CA2+ SIGNALS IS CONTROLLED BY THE STOICHIOMETRY OF MICU1/2 AND MCU. Mohammed Mostafizur Rahman, Institute for Stem Cell Biology and Regenerative Medicine, India, STRESS-INDUCED DIFFERENTIAL REGULATION LEADS TO DECOUPLING OF THE ACTIVITY BETWEEN MPFC AND AMYGDALA. Marcin Wolny, University of Leeds, United Kingdom, DESIGN AND CHARACTERIZATION OF LONG AND STABLE DE NOVO SINGLE α-HELIX DOMAINS. Elvis Pandzic, University of New South Wales, Australia, VELOCITY LANDSCAPES RESOLVE MULTIPLE DYNAMICAL POPULATIONS FROM FLUORESCENCE IMAGE TIME SERIES. The Biophysical Society, founded in 1958, is a professional, scientific Society established to encourage development and dissemination of knowledge in biophysics. The Society promotes growth in this expanding field through its annual meeting, monthly journal, and committee and outreach activities. Its 9000 members are located throughout the U.S. and the world, where they teach and conduct research in colleges, universities, laboratories, government agencies, and industry. For more information on these awards, the Society, or the 2017 Annual Meeting, visit http://www.

Tsupykov O.,Bogomoletz Institute of Physiology | Tsupykov O.,State Institute of Genetic and Regenerative Medicine
Microscopy Research and Technique | Year: 2015

Despite the great number of studies devoted to neural stem/progenitor cell biology, the ultrastructural characteristics of these cells in vitro have not been fully studied. To determine the fine structure of hippocampal neural progenitor cells (NPCs) in culture, mouse fetal hippocampi (E18) were extracted, dissected, and cells were expanded as adherent monolayer culture. Electron microscopy revealed that NPCs had an immature phenotype, with a high nuclear/cytoplasmic ratio, small and scant organelles, underdeveloped endoplasmic reticulum, and many free ribosomes and polysomes. Our results may contribute to a better understanding of the fine structure and physiology of hippocampal NPCs in vitro. © 2014 Wiley Periodicals, Inc.

Skibo G.G.,Bogomoletz Institute of Physiology
Vitamins and hormones | Year: 2010

Brain plasticity describes the potential of the organ for adaptive changes involved in various phenomena in health and disease. A substantial amount of experimental evidence, received in animal and cell models, shows that a cascade of plastic changes at the molecular, cellular, and tissue levels, is initiated in different regions of the postischemic brain. Underlying mechanisms include neurochemical alterations, functional changes in excitatory and inhibitory synapses, axonal and dendritic sprouting, and reorganization of sensory and motor central maps. Multiple lines of evidence indicate numerous points in which the process of postischemic recovery may be influenced with the aim to restore the full capacity of the brain tissue injured by an ischemic episode. Copyright 2010 Elsevier Inc. All rights reserved.

Krishtal O.,Bogomoletz Institute of Physiology
Neuropharmacology | Year: 2015

The history of ASICs began in 1980 with unexpected observation. The concept of highly selective Na(+) current gated by specific receptors for protons was not easily accepted. It took 16 years to get these receptor/channels cloned and start a new stage in their investigation. "The receptor for protons" became ASIC comprising under this name a family of receptor/channels ubiquitous for mammalian nervous system, both peripheral and central. The role of ASICs as putative nociceptors was suggested almost immediately after their discovery. This role subsequently was proven in many forms of pain-related phenomena. Many other functions of ASICs have been also found or primed for speculations both in physiology and in disease. Despite the width of field and strength of efforts, numerous basic questions are to be answered before we understand how the local changes in pH in the nervous tissue transform into electric and messenger signaling via ASICs as transducers. This article is part of the Special Issue entitled 'Acid-Sensing Ion Channels in the Nervous System'. Copyright © 2015. Published by Elsevier Ltd.

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